Inward-rectifier K+ current in guinea-pig ventricular myocytes exposed to hyperosmotic solutions.

Superfusion of heart cells with hyperosmotic solution causes cell shrinkage and inhibition of membrane ionic currents, including delayed-rectifer K+ currents. To determine whether osmotic shrinkage also inhibits inwardly-rectifying K+ current (I(K1)), guinea-pig ventricular myocytes in the perforated-patch or ruptured-patch configuration were superfused with a Tyrode's solution whose osmolarity (T) relative to isosmotic (1T) solution was increased to 1.3-2.2T by addition of sucrose. Hyperosmotic superfusate caused a rapid shrinkage that was accompanied by a negative shift in the reversal potential of Ba(2+)-sensitive I(K1), an increase in the amplitude of outward I(K1), and a steepening of the slope of the inward I(K1)-voltage (V) relation. The magnitude of these effects increased with external osmolarity. To evaluate the underlying changes in chord conductance (G(K1)) and rectification, G(K1)-V data were fitted with Boltzmann functions to determine maximal G(K1) (G(K1)max) and voltage at one-half G(K1)max (V(0.5)). Superfusion with hyperosmotic sucrose solutions led to significant increases in G(K1)max (e.g., 28 +/- 2% with 1.8T), and significant negative shifts in V(0.5) (e.g., -6.7 +/- 0.6 mV with 1.8T). Data from myocytes investigated under hyperosmotic conditions that do not induce shrinkage indicate that G(K1)max and V(0.5) were insensitive to hyperosmotic stress per se but sensitive to elevation of intracellular K+. We conclude that the effects of hyperosmotic sucrose solutions on I(K1) are related to shrinkage-induced concentrating of intracellular K+.